Gregory Cochran's "gay germ" hypothesis posits that male homosexuality is likely caused by a germ.
- The low hereditability of homosexuality (0.22) 
- The absence of homosexuality in hunter-gatherer populations
- The relatively high frequency of homosexuality (~4% in the West, and growing)
- The lack of any plausible evolutionary explanation.
A male lack of sexual interest in females would be an evolutionary penalty. If it were genetic, the trait would have been selected out long ago because of a lack of reproductive fitness. Also, the frequency is too high to be caused by a mutation.
There are various examples of infectious agents altering behavior: 
- Rabies causes dogs to be more aggressive in the final stage of the disease.
- Influenza causes humans to be more social in the days prior to the noticeable effects.
- Toxoplasma (see below) causes rats to be (sexually) attracted to cat urine;
Consider that there is already a known similar germ,
A microscopic parasite whose contagion is called "Toxoplasmosis". It is thought to be able to infect all warm blooded animals (including humans), but particularly infects rats, rewires their brain to not only stop fearing cats (a natural predator), but also become sexually attracted to cat urine. The parasite does this because it (Toxoplasma gondii) can only reproduce inside of cat guts, so it changes the host-rat's behavior to get the rat eaten by cats so that the parasite can reproduce (to the detriment of the rat). Stated again for emphasis, it's already proven that microorganisms can reprogram warm-blooded animals' sexual attraction. And it is already proven that humans are not immune to this specific microorganism (we do not know all of its effects in humans yet).
Given that there are many more examples of behavior-altering agents (mostly viruses), this leads to the conclusion that a pathogen changing sexual orientation is far from impossible. It would explain the frequency in Western populations and the absence in hunter-gatherers.
Toxoplasma gondii is a parasite. According to at least one scientific study, homosexual males are fightiningly more likely to have parasites than heterosexuals (~70% vs 16%).
Furthermore, there is the interesting phenomenon of homophobia. Homophobia isn't an actual phobia, but an aversion of gays. Interestingly, homophobia actually is heritable, much more so than homosexuality (~0.5). If it is heritable, what purpose does it serve? In particular, what purpose does it serve if homosexuality is caused by a pathogen?
Research has been done on the nature of homophobia, and this research has found that it
exists strongest with regard to homosexuals' contact with children.
A subjective 'degree of discomfort' was found much higher when confronted with a scenario
of gay people who hold a profession that involved contact with children (such as pediatrician or teacher)
than with gay people who were e.g. lawyers or construction workers.
A second study showed that for different types of medical doctors,
a high degree of contact with children (e.g. child psychiatrist) induced more discomfort than an
invasive procedure (e.g. brain surgeon) but only for gay doctors.
Two more studies clearly suggested that homophobia is aimed at preventing children,
particularly younger children, from being exposed to homosexuals.
Is it not plausible that homophobia is aimed at preventing the spread of the pathogen that causes homosexuality?
Cochran asserts that it’s not likely that the pathogen is spread by homosexual sex. How the putative pathogen is spread is not clear at this time. Even less clear is whether there is a “critical period” for this infection to affect sexual orientation. It’s also not clear how prevalent the pathogen is in the population, or what percentage of infected individuals become homosexual.
Regardless of how the pathogen is spread, it likely that extended periods of fairly close contact with an infected individual is more likely to result in transmission of the infectious agent. If there is a critical period of time, say some time in childhood, for an infection to result in sexual orientation being altered, the evolutionary purpose of homophobia starts to become more apparent.
Indeed, the existence of homophobia may stand as pretty good evidence in support of Greg Cochran’s pathogenic hypothesis for homosexuality. Indeed, for as many have pointed out, homosexuals are otherwise harmless and indeed perhaps beneficial to other males in the group (reduced competition for females, for example). That gays are nonetheless hated seems hard to explain otherwise.
One possible way to test Cochran’s hypothesis is to observe if there is a higher incidence of homosexuality among the adopted children of homosexuals. Using adoptees controls for heredity, and presumably, sharing a household should give plenty of opportunity for the pathogen to be passed on to the adopted child. Ideally, the study should look only at children adopted very young, from strangers (to minimize selection bias among the adopted children). If higher rates of homosexuality were observed among these adopted children, it would point to some environmental factor – the most likely being infection.
The low, but non-zero heritability of male homosexuality may be indicative of some sort of genetic susceptibility to the pathogen, perhaps through weakened defenses or a vulnerable neural architecture.
If homosexuality is indeed caused by an infectious agent, it would have broad implications for society, particularly the prospect of being able to prevent homosexuality (perhaps through a vaccine) if one desires it.
US CDC webpage on toxoplasmosis
- Estimated that 11% of Americans aged 6 or older have been infected
- Infected-Cat to Human (typically via feces)
- Congenital (pregnant mother to unborn child)
- Foodborne (typically via undercooked meats)
Webster, Joanne P, and Glenn A McConkey.
“Toxoplasma gondii-altered host behaviour: clues as to mechanism of action.”
Folia parasitologica vol. 57,2 (2010): 95-104. doi:10.14411/fp.2010.012
- A convincing body of evidence now exists, from both human and animal studies, to indicate that Toxoplasma gondii can cause specific behavioural changes in its host, likely to be the product of strong selective pressures for the parasite to enhance transmission from its intermediate host reservoir, primarily rodent, to its feline definitive host, wherein sexual reproduction can occur and the parasite's life cycle completed.
Webster, Joanne P.
“The effect of Toxoplasma gondii on animal behavior: playing cat and mouse.”
Schizophrenia bulletin vol. 33,3 (2007): 752-6. doi:10.1093/schbul/sbl073
- A convincing body of evidence now exists that Toxoplasma gondii can cause permanent behavioral changes in its host, even as a consequence of adult-acquired latent infection.
- Such behavioral alterations appear to be the product of strong selective pressures for the parasite to enhance transmission from its intermediate host reservoir, primarily rodent, to its feline definitive host, wherein sexual reproduction can occur and the life cycle completed.
- Extensive studies carried out under different experimental conditions suggest that T. gondii changes the behavior of rodents so as to make them more likely to be predated on by cats, the parasite's definitive host.
Xiao, J et al.
“Sex-specific changes in gene expression and behavior induced by chronic Toxoplasma infection in mice.”
Neuroscience vol. 206 (2012): 39-48. doi:10.1016/j.neuroscience.2011.12.051
- There is growing evidence that Toxoplasma gondii modifies the behavior of its intermediate hosts.
- Results indicate that the sex of the host (the mammal infected) plays a major role in determining variable brain and behavior changes following Toxoplasma infection. These observations are consistent with heterogeneity of neuropsychiatric outcomes of the infection in humans.
- Gene expression signatures were generated in the frontal cortex of male and female mice during latent stage of infection.
- In female mice, infection caused attraction to cat odor, altered the expression of genes involved in the development of the forebrain, neurogenesis, and sensory and motor coordination.
- In male mice, infection led mainly to modulation of genes associated with olfactory function (including downregulation of a number of olfactory receptors and dopamine receptor D4).
Berdoy, M et al.
“Fatal attraction in rats infected with Toxoplasma gondii.”
Proceedings. Biological sciences vol. 267,1452 (2000): 1591-4. doi:10.1098/rspb.2000.1182
- T. gondii's manipulation appears to alter the rat's perception of cat predation risk, in some cases turning their innate aversion into an imprudent attraction.
Vyas, Ajai et al.
“Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors.”
Proceedings of the National Academy of Sciences of the United States of America vol. 104,15 (2007):
- In mice and rats, latent infection converted the aversion to feline odors into attraction. Such loss of fear is remarkably specific.
“Parasite gives wolves what it takes to be pack leaders.”
Nature, 10.1038/d41586-022-03836-9. 24 Nov. 2022, doi:10.1038/d41586-022-03836-9
- Wolves infected with T. Gondii are more likely than uninfected ones to lead a pack. Infected animals are also more likely to leave their home packs and strike out on their own.
Meyer, C.J., Cassidy, K.A., Stahler, E.E. et al.
Parasitic infection increases risk-taking in a social, intermediate host carnivore.
Commun Biol 5, 1180 (2022). https://doi.org/10.1038/s42003-022-04122-0
- Results suggest that wild wolves contract toxoplasma gondii directly from cougars (where said infection breeds) or their oocysts or scat.
- Toxoplasma gondii infection in wild wolves strongly coorelated with (presumably causing) high-risk decisions such as becoming a pack leader and dispersing (often exploring new habitats and are the individuals expanding current gray wolf range).
- Infected wolves were 11 times more likely than uninfected ones to leave their birth family to start a new pack, and 46 times more likely to become pack leaders — often the only wolves in the pack that breed.
- The suspected feedback loop is that these adventuring infected wolves are more likely to become pack leaders and/or breeders lead uninfected wolves to cougars where both the virus can get back to cougars for the virus to reproduce, and for more wolves to get infected.
Poirotte, Clémence et al.
“Morbid attraction to leopard urine in Toxoplasma-infected chimpanzees.”
Current biology : CB vol. 26,3 (2016): R98-9. doi:10.1016/j.cub.2015.12.020
- Linked to increased risk-taking in chimpanzees.
Gering, Eben et al.
“Toxoplasma gondii infections are associated with costly boldness toward felids in a wild host.”
Nature communications vol. 12,1 3842. 22 Jun. 2021, doi:10.1038/s41467-021-24092-x
- Linked to increased risk-taking in hyenas.
Audrey Lim, Vineet Kumar, Shantala A Hari Dass, Ajai Vyas
“Toxoplasma gondii infection enhances testicular steroidogenesis in rats.”
Molecular ecology vol. 22,1 (2013): 102-10. doi:10.1111/mec.12042
- In rats, infection enhances expression of genes involved in facilitating synthesis of testosterone (known to reduce fear and enhance sexual attractiveness in males), resulting in greater testicular testosterone production.
Zouei, Nima et al.
“The association of latent toxoplasmosis and level of serum testosterone in humans.”
BMC research notes vol. 11,1 365. 8 Jun. 2018, doi:10.1186/s13104-018-3468-5
- Humans infected have statistically-significantly more testosterone.
Johnson, Stefanie K et al.
“Risky business: linking Toxoplasma gondii infection and entrepreneurship behaviours across individuals and countries.”
Proceedings. Biological sciences vol. 285,1883 20180822.
25 Jul. 2018, doi:10.1098/rspb.2018.0822
- ~2 billion humans worldwide infected and has been linked to behavioural alterations in humans and other vertebrates
- Among professionals attending entrepreneurship events, T. gondii-positive individuals were 1.8× more likely to have started their own business compared with other attendees. Infection prevalence was a consistent, positive predictor of entrepreneurial activity and intentions at the national scale, regardless of whether previously identified economic covariates were included.
Borráz-León, Javier I et al.
“Are Toxoplasma-infected subjects more attractive, symmetrical, or healthier than non-infected ones?
Evidence from subjective and objective measurements.”
PeerJ vol. 10 e13122. 25 Mar. 2022, doi:10.7717/peerj.13122
- Infected men had more attractive faces. Infected women had lower body mass, lower body mass index, more attractive faces, higher self-perceived attractiveness, and a higher number of sexual partners.
- Infected men and women were rated as more attractive and healthier than non-infected ones.
Flegr, Jaroslav et al.
“Increased risk of traffic accidents in subjects with latent toxoplasmosis:
a retrospective case-control study.”
BMC infectious diseases vol. 2 11. 2 Jul. 2002,
- Humans infected have significantly (2.65x) increased risk of traffic accidents. Relative risk of traffic accidents decreases with the duration of infection.
“Toxoplasmosis and behavioural changes.”
Journal francais d'ophtalmologie vol. 43,3 (2020): e89-e93.
- Infection is classically associated with the frequency of schizophrenia, suicide attempts or "road rage".
- Infection prevalence was a consistent, positive predictor of entrepreneurial activity